No abstract available.
Cytarabine* ; Drug Therapy, Combination* ; Leukemia, Myeloid, Acute*

No abstract available.
Lymphoma, T-Cell, Cutaneous*

The search for tumor-avid agents for use in nuclear medicine imaging is an ongoing field of importance. The purpose of this study was to determine the affinity for radiolabeled vitamin B12 by a wide histologic variety of tumor types in mice. Seventeen different types of tumor were grown subcutaneously in female Balb/C or Balb nu/nu(nude) mice. When the tumors reached about 1 cm in diameter, mice were injected intraperitoneally with 57Co-vitamin B12. Twenty-foul hours later, the mice were sacrificed. Organs and tissues were removed, weighed, and activity per mg determined by gamma counter. Values represented cpm/mg tissue that was normalized to 20 grams body weight for each mouse. A wide variety of tumor types showed significant uptake and concentration of 57Co-vitamin B12, as evidenced by tumor:tissue activity ratios. For many tissues of great importance in terms of background(bone, muscle, blood), the tumor:tissue activity ratios of uptake were high. These data strongly suggest that further efforts to evaluate the utility of radiolabeled adducts of vitamin B12 for clinical use in oncologic imaging are warranted.
Animals ; Body Weight ; Female ; Humans ; Mice* ; Nuclear Medicine ; Vitamin B 12

No abstract available.
Pericardial Effusion* ; Radionuclide Imaging* ; Technetium Tc 99m Medronate*

Retroperitoneal cystic lymphangiomas are uncommon tumors usually found incidentally at surgery, autopsy, orlymphography. When clinically significant, they usually present early in life as a palpable abdominal mass. Wediscribe an unusual case of a six-years old boy who was operated for a cystic lymphangioma of the right axilla atthe age of five months, and, six years later, was found to have a retroperitoneal cystic lymphangioma accompainedwith motor weakness of the lower extremities.
Autopsy ; Axilla ; Humans ; Lower Extremity ; Lymphangioma, Cystic ; Male

PURPOSE: Metallothionein is an intracellular cystein-rich thiol-containing protein. Increased metallothionein content in tumor cells has been suggested to be a mechanism of resistance to cisplatin. In most of previous studies evaluating the role of metallothionein in cisplatin resistance, tumor cells were usually exposed to cadmium to increase metallothionein content. Therefore, cisplatin resistance of the cells may be related to cadmium exposure itself, which induces various changes in cell characteristics, but not to increased metallothionein content. The purpose of this study is to evaluate the role of metallothionein content alone in cellular resistance to cisplatin without exposure of cells to cadmium. MATERIALS AND METHOD: We measured the toxicity of cisplatin in mouse NIH/3T3 cells that vary in their content of metallothionein as a consequence of transfection with a plasmid that result in the constitutive expression of metallothionein. MT cells were derived from NIH/3T3 cells by transfection with a plasmid containing the genome of bovine papilloma virus and the mouse metallothionein-I, derived by the promoter for the glucose-regulated protein of 78kD. Control cells were similary transfected with bovine papilloma virus-based plasmids with the gene for metallothionein inverted and thus separated from the promoter (TM), or deleted, along with promoter (BPA). The number of copies of the plasmid were similar in each kind of transfected cells. Expression of metallothionein required neither selection nor maintenance of cells in the presence of heavy metals. RESULTS: Synthesis of metallothionein was 15-fold greater in the MT cells than in the TM or BPA cells. The concentration of cisplatin sufficient to reduce the cells per well by one-half (IC-50) was 0.40+/-0.075 uM in MT cells. In TM and BPA cells, it was 0.36 0.035 uM and 0.423+/-0.032 uM. There were no significant differences in IC-50 between three cell lines. CONCLUSION: In spite of large differences between MT and control cells in their cellular content of metallothionein, no differences in resistance to cisplatin were observed.
Animals ; Cadmium ; Cell Line ; Cisplatin* ; Genome ; Metallothionein* ; Metals, Heavy ; Mice* ; Papilloma ; Plasmids ; Transfection

No abstract available.
Glomerulonephritis, IGA* ; Hodgkin Disease* ; Immunoglobulin A*

The heart was considered to be relatively resistant to ionizing irradiation in the range of doses used in radiation therapy before follow up and review of a large number of patients who had undergone mediastinal irradiation and survived for several years. Cardiac complications after mediastinal irradiation include coronary artery disease, valvular heart disease, and acute and chronic pericardial disease. Pericarditis and pericardial effusion have been regarded as the most common side effects of cardiac irradiation. However, modern techniques of irradiation, dose fractionation, and reduction of the heart volume irradiated in most malignancies have substantially reduced the frequency of cardiac complications including pericarditis. Therefore, effusive- constrictive or constrictive pericarditis is less often noted after the completion of radiation therapy. Delayed appearance of effusive-constrictive pericarditis after mediastinal irradiation has not been commonly recognized by physicians. We recently experienced a case of delayed pericarditis with effusion occurring 36 months after radiation therapy for young patient with Hodgkin's disease. Mediastinal irradiation for Hodgkin's disease increases the risk of subsequent death from heart disease. Risk increased with high mediastinal doses, minimal protective cardiac blocking, young age at irradiation, and increasing duration of follow-up. Consequently, the current practice of using a subcarinal block and multiple portals, with irradiation through both anterior and posterior fields, may be expected to lead to a decline in the incidence and severity of cardiac abnormality after irradiation.
Cardiac Volume ; Coronary Artery Disease ; Dose Fractionation ; Follow-Up Studies ; Heart ; Heart Diseases ; Heart Valve Diseases ; Hodgkin Disease* ; Humans ; Incidence ; Pericardial Effusion ; Pericarditis* ; Pericarditis, Constrictive

Nitric oxide (NO) is emerging as a potential anti-cancer agent to overcome tumor cell resistance to conventional therapeutic agents. NO is a short-life molecule produced from L-arginine by the nitric oxide synthase (NOS). There are three isoforms of the enzyme: neuronal NOS (nNOS or NOS1), inducible NOS (iNOS or NOS2), and endothelial NOS (eNOS or NOS3). Each of these isoforms may be expressed in a variety of cell types. The actions of NO are highly variable in oncology revealing both sides of the spectrum as an anti-neoplastic versus a pro-neoplastic agent. The final activity of NO is dependent on its working microenvironment, including the type of cell exposed to NO, the redox state of the reaction, as well as the final intracellular concentration and the duration of exposure to NO. NO donors mimic continuous production of NO in a wide range of time intervals (seconds to days). Thus, multiple biological and (pro- versus anti-) neoplastic responses are elicited from NO donors depending on the half-life and the type of cell exposed to the compound. This paper is a review of the current knowledge of various roles of NO in cancer.
Arginine ; Half-Life ; Humans ; Hydrazines ; Neurons ; Nitric Oxide ; Nitric Oxide Synthase ; Oxidation-Reduction ; Protein Isoforms ; Tissue Donors

No abstract available.
Hypertension, Renovascular* ; Pheochromocytoma*